Acidosis and contractility of heart muscle.
The contractility of heart muscle is sensitive to small and physiological changes of extracellular pH. The reduction of contractility associated with an acidosis is determined by the fall of pH in the intracellular fluid. The function of many organelles within the cardiac cell is affected by hydrogen ions. The tension generated by isolated myofibrils at a fixed calcium concentration is reduced at low pH. The dominant mechanism for the reduction of contractility in whole tissue is competitive inhibition of the slow calcium current by hydrogen ions. The reduction of the slow calcium current is similar when the same fall of developed tension is induced by acidosis or by a reduction of extracellular calcium concentration. Measurement of tissue pH with fast-responding extracellular electrodes show that, in myocardial ischaemia, tissue acidosis develops at the same time or only seconds before the onset of contractile failure. Much of the reduced contractility can be accounted for by the severity of the acidosis. Although a mild acidosis can delay or prevent damage to the myocardium from ischaemia or hypoxia, a severe acidosis is not beneficial and may even cause tissue necrosis.
D000138:Acidosis / Q000503:physiopathology*; D000142:Acidosis, Respiratory / Q000503:physiopathology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002245:Carbon Dioxide / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism; D004058:Diffusion; D006859:Hydrogen / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism; D007424:Intracellular Fluid / Q000032:analysis; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D009210:Myofibrils / Q000378:metabolism; D009336:Necrosis; D012508:Sarcolemma / Q000378:metabolism
D001639:Bicarbonates; D002245:Carbon Dioxide; D006859:Hydrogen; D002118:Calcium